Impact of in-stent restenosis on death and myocardial infarction.

Although drug-eluting stents reduce restenosis and target lesion revascularization compared with bare metal stents (BMSs), the specter of late stent thrombosis has curbed enthusiasm for the widespread use of drug-eluting stents. Alternatively, increasing BMS use would increase restenosis and potentially increase adverse events. The presentation and outcomes of BMS restenosis are controversial. We evaluated 2,539 patients with BMS restenosis referred for repeat revascularization. Major adverse cardiac events, including mortality and myocardial infarction (MI), were assessed at clinical presentation, 30 days, and 6 months. Patients with acute presentation (i.e., unstable angina requiring hospitalization or MI) were compared with patients with stable presentation. At presentation, 19.2% of patients were asymptomatic, 27.5% had exertional angina, 46.6% had unstable angina, and 6.7% had MI. Mortality and MI rates were 1.1% and 1.4%, respectively, at 30 days and 3.3% and 4.5%, respectively, at 6 months. Patients with acute coronary syndrome (ACS) and those without ACS had similarly low mortality rates at 30 days (1.2% ACS vs 1.0% non-ACS, p = 0.65) and 6 months (3.4% ACS vs 3.3% non-ACS, p = 0.93) and MI rates at 30 days (1.3% ACS vs 1.4% non-ACS, p = 0.87) and 6 months (4.7% ACS vs 4.3% non-ACS, p = 0.65). Combined major adverse cardiac events were similar at 30 days (2.5% vs 2.1%, p = 0.53) and 6 months (7.4% ACS vs 6.9%, non-ACS, p = 0.65). In conclusion, although BMS restenosis often manifests as an ACS, it is associated with a low incidence of 6-month major adverse cardiac events and does not predict a negative outcome.

Treatment of drug-eluting stent restenosis with the same versus different drug-eluting stent.

OBJECTIVE: The authors aimed to compare the clinical outcomes with repeat drug-eluting stent (DES) implantation utilizing the same type versus an alternate DES type for in-stent restenosis (ISR) of DES. BACKGROUND: : DES are proven as an effective treatment for bare metal ISR. METHODS: A cohort of 116 patients previously treated with a sirolimus-eluting stent (SES) or a paclitaxel-eluting stent (PES) who presented with angiographic ISR were treated with repeat DES. Of these, 62 (53.4%) were treated with different DES and 54 (46.6%) were treated with the same DES. This cohort was followed for clinical events at 30 days, 6 months, and 1 year. RESULTS: Baseline characteristics were similar except for more diabetes among patients receiving the different type of DES. Of the 116, overall 16.4% of the DES were implanted for previous ISR and 2.6% had previously received brachytherapy. At 6 months, the overall target vessel revascularization (TVR) rate was 12.2% for the entire cohort. The TVR-major adverse cardiac event (MACE) rate for the patients treated with different DES was 14.5% and 16.7% for the same DES (P = 0.750). Overall TVR rate at 1 year was 28.8%. The TVR-MACE was 32.6% for different DES and 35.0% for the same DES (P = 0.814). CONCLUSIONS: Reimplantation of DES for the treatment of DES ISR (same or different) is safe but associated with a high rate of recurrences at 1 year regardless of the initial DES type. Other treatment modalities for ISR of DES should be considered to further improve the overall TVR-MACE.

Role of angiotensin receptor blockers in the prevention and treatment of arrhythmias.

The renin-angiotensin system is a key regulatory system that is activated in many forms of cardiovascular disease. It is well established that angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are important therapeutic agents in the treatment of hypertension, myocardial infarction, and congestive heart failure. More recent research has suggested that renin-angiotensin system activation may also play a critical role in the genesis of atrial and ventricular arrhythmias. The possible role of renin-angiotensin system activation in arrhythmogenesis suggests that ACE inhibitors and ARBs may be important therapeutic agents in the prevention and treatment of arrhythmias. This review summarizes the current evidence for the use of ARBs in the treatment of atrial and ventricular arrhythmias.

Apoptosis and heart failure: clinical relevance and therapeutic target.

Heart failure is the final common pathway of diverse etiologies that are characterized by impaired systolic and/or diastolic function with high morbidity and mortality. An integral part of pathogenesis of heart failure is myocyte loss. The traditional explanation for myocyte loss was cell necrosis but over the last decade, there has been a surge of evidence affirming the role of apoptosis in genesis of heart failure. Studies have raised apoptosis from a 'histologic curiosity' to an exciting 'clinical target' that can be modulated to attenuate the progression of heart failure. This review will focus on the clinical relevance of apoptosis in human and experimental heart failure and identify some of the progress made in myocardial anti-apoptotic intervention.

Apoptosis as a therapeutic target in acutely ischemic myocardium.

In addition to necrosis, apoptosis makes a significant contribution to cell death following acute myocardial ischemia; apoptosis is particularly enhanced during reperfusion. Several studies are beginning to indicate that the cell death by apoptosis may be preventable. A boost in the research in this direction has been provided by noninvasive means of detection of apoptosis, such as that achieved by technetium-99m labeled Annexin-A5 scintigraphy. Various levels within the apoptotic cascade are being investigated as therapeutic targets. Caspase inhibitors, mitochondrial stabilizers, and Na+-H+ exchanger inhibitors reduce cell death by apoptosis and infarct size. Although most of the evidence at present is limited to the laboratory animals, this approach seems to hold a promise for the future.

Pathogenetic basis of myocardial dysfunction and amenability to reversal.

As the role of the LVAD graduates from the "bridge-to-transplant" to the "bridge-to-recovery," several important issues need to be answered. Such a paradigm would require a definition of appropriate candidates for LVAD implantation, the most appropriate time for LVAD placement during the management of end-stage CHF, reliable histologic, biochemical, and imaging markers of recovery, and the optimum duration of LVAD support. The device technology must be refined further to reduce the morbidity associated with the device itself, and to make the device smaller, less invasive, and less thrombogenic. It will be a challenge to identify the role for concomitant drug therapy and to develop weaning programs for device support. Finally, guidelines will have to be developed to monitor and manage these patients after explantation of LVAD.